Vaskulopatija srčanog presadka

Cardiac allograft vasculopathy (CAV) is a disease characterized by endothelial dysfunction, intimal thickening of coronary arteries with subsequent ischaemia and failure of the transplanted heart. CAV is one of the major determinants of longterm survival in cardiac transplant patients with an incidence of 48% at 10 years. The disease evolves from a complex interplay between both immunological and non-immunological factors, some being ”classical” atherosclerotic risk factors. Clinical diagnosis can be very difficult since these patients present with atypical symptoms of myocardial ischemia, no angina because of graft denervation, or often no symptoms at all. Instead the initial presentation is often progressive heart failure or sudden death making screening methods vital to detect the disease early. The standardized diagnostic and screening tool for the clinical practice is currently coronary angiography, although positive predictive value is only 44% when compared to intravascular ultrasound as the gold standard. Another a major disadvantage of angiography is the risk of developing contrast nephropathy since many of these patients have renal dysfunction from immunosuppressive treatment. While CAV generally is a slowly progressive disease, effective prevention and treatment methods are lacking and hence the disease carries a poor prognosis. Statins and mTOR inhibitors are key players in both prevention and treatment and are part of the standard drug regime for all patients. In addition to medical treatment, revascularization therapy is also possible in a very small subgroup of patients. However, revascularization is considered palliative and is not proven to prolong graft survival. Implantable cardioverterdefibrillator (ICD) devices are used in advanced stages but is not evidence-based for CAV in particular. Unfortunately the only definite and ultimate treatment option is retransplantation. New treatment methods are clearly needed.Vaskulopatija srčanog presadka (VSP) je bolest karakterizirana disfunkcijom endotela, zadebljanjem intime koronarnih arterija s posljedičnom ishemijom i zatajivanjem transplantiranog srca. VSP je jedna od glavnih determinanata dugoročnog preživljavanja u srčanih transplantiranih bolesnika s učestalosti od 48% nakon 10 godina. Bolest se razvija iz složenih međudjelovanja između imunoloških i neimunoloških faktora, od kojih su neki „klasični“ faktori aterosklerotskog rizika. Klinička dijagnoza može biti vrlo zahtjevna jer se ovi bolesnici prezentiraju atipičnim simptomima ishemije miokarda, bez angine zbog denervacije presadka, ili su često potpuno bez simptoma. Progresivno popuštanje presadka ili iznenadna smrt su nerijetko prve manifestacije ove bolesti, učinivši metode probira bitnima u ranom otkrivanju bolesti. Standardni alat u dijagnostici i probiru u kliničkoj praksi je trenutno koronarna angiografija, makar joj je pozitivna prediktivna vrijednost samo 44% kada se usporedi s intravaskularnim ultrazvukom kao zlatnim standardom. Još jedna nepovoljna osobina angiografije je rizik od razvoja kontrastne nefropatije s obzirom da mnogo ovih pacijenata ima renalnu disfunkciju zbog imunosupresivne terapije. Iako je VSP generalno sporo progredirajuća bolest, nedostaju učinkovite metode prevencije i liječenja te je zbog toga bolest povezana s lošom prognozom. Statini i inhibitori mTOR-a su za sada ključni u prevenciji i liječenju te su dio standardnog režima lijekova za sve pacijente. Uz lijekove, terapija revaskularizacijom je također moguća u relativno maloj podgrupi bolesnika. Međutim, revaskularizacija se smatra palijativnom metodom te nije dokazano da produžuje preživljavanje presadka. Implantabilni kardioverter-defibrilator (ICD) se često koristi u uznapredovalim stadijima VSP, iako bez koristi utemeljene dokazima. Nažalost, jedina preostala definitivna opcija liječenja jest ponovna transplantacija. Više je nego očito da trebamo nove i učinkovitije metode liječenja